Phthalate exposure alters heart muscle cell behaviour and could lead to heart disease

Phthalates, as plasticisers, are ubiquitous in the environment, found in everyday objects such as cosmetics, packaging, pharmaceutical pills, children’s toys, shampoos, detergents etc. In fact, phthalates are so pervasive that measurable levels of many metabolites are found in the urine of the general American population.

Phthalates are easily leached into the environment due to its structure; the process  is hastened as plastics age and breakdown. Exposure of humans occurs largely through diet and through contact with phthalate containing materials.

Phthalate exposures in laboratory animals have been show to affect the reproductive system leading to disruptions of hormones and could be endocrine disruptors. Phthalates have also been linked to behavioral disorders in children.  Previously in our blog, we discussed how phthalate exposure in expectant mothers could lead to aggression, conduct problems, attention problems, and depression in children. Now a new study by scientists from George Washington University, USA, explored the effect of a phthalate Diethylhexyl phthalate (DEHP)  on cardiomyocytes (cells that comprise the heart muscles). DEHP is found in a range of products such as  building materials, medical devices, paints and adhesives and also found in food products due to leaching during food production and storage. The researchers found that  Di(2-ethylhexyl)phthalate (DEHP ) can cause changes in metabolic processes in the cardiomyocytes by increasing the genes that are involved in the transport of fatty acids, oxygen consumption etc.

 So what are the implications of this finding?  Dependence of the cardiomyocytes to fatty acids for energy production could lead to an abundance of lipid intermediates and reactive oxygen species. Phthalate induced change in the heart muscle cells could lead the heart  to be sensitive to injury caused by reduced oxygen and also cause dysfunction of ventricles which could lead to a range of heart diseases resulting in heart failure. 

References:

Posnack NG, Swift LM, Kay MW, Lee NH, & Sarvazyan N (2012). Phthalate Exposure Changes the Metabolic Profile of Cardiac Muscle Cells. Environmental health perspectives PMID: 22672789

Computer, computer, on a desk, Who is the greenest of fonts all?

We are humans, with our own unique quirks. This quirkiness also exhibits itself in our typeset of preference. For instance, Garamond is my favourite since it is neat and very comfortable to read (and, indeed, I have experimented with all fonts on Word, including MT Extra and the various Wingdings)- admittedly, the Oxonian in me often shifts towards Perpetua. But a curiosity to know more about the fonts made me stumble against something else- green fonts!


So, these are those which use less ink and paper when printing, conditional on the font size used. There are quite a many contenders for the title of greenest font. Those suggested so far are Century Gothic (font size: 10) which is supposedly better than Ecofont (font size: 10) but loses out on the paper front since the font itself is wide. This is followed by Times New Roman (font size: 11), Calibri (11), Verdana (10), Arial (11), Sans serif (11), Trebuchet (11), Tahoma (11), and Franklin Gothic Medium (11). However, Matt Robinson and Tom Wrigglesworth identified Garamond as fitting the bill.

I conducted a little experiment using normal fonts (i.e unitalicised or not bold or too narrow/wide), all size 11, from MS Office 2007 - the purpose, after all, is to write/print something readable! I have deliberately included the ruler from MS Word so that you can judge its dimensions. I apologise for the rudimentary photo- this was made using Windows Paint since I no longer have access to Adobe Photoshop.

I await your thoughts!

Diesel engine exhausts does indeed cause cancer in humans

In an earlier post, Sarah Stephen (April 2012, http://ecoratorio.blogspot.co.uk/2012/04/minefield-of-diesel-emissions.html ) wrote about diesel fuel emissions, its health effects, and the impending International Agency for Research on Cancer (IARC) meeting scheduled for June 2012 at which the labelling of diesel engine exhausts would be evaluated.

IARC is an intergovernmental agency which is part of the World Health Organisation with the role of conducting and coordinating research into the causes and prevention of cancer. The organisation places emphasis on understanding the role of environmental and lifestyle risk factors and studying their interplay with genetic factors in population-based studies and relevant experimental models. A major thrust of the organisation is the IARC Monographs Programme where international experts evaluate the evidence of the carcinogenicity (cancer causing property) of environmental factors.

IARC classifies environmental factors in 5 groups:

• Group 1 - Carcinogenic to humans

• Group 2A - Probably carcinogenic to humans

• Group 2B - Possibly carcinogenic to humans

• Group 3 - Not classifiable as to its carcinogenicity to humans

• Group 4 - Probably not carcinogenic to humans

Over 900 environmental agents have been evaluated by IARC since 1971 of which more than 100 have been identified as carcinogenic to humans (Group 1), and more than 300 as probably carcinogenic, or possibly carcinogenic to humans (Groups 2A, 2B).

As early as 1988, the experts at IARC classified diesel exhaust as ‘probably carcinogenic’

(carcinogenic- that which can cause cancer) to humans. Now, nearly 25 years later, after the emergence of a compelling study that occupational exhaust of miners predisposed them to lung cancer (Silverman et al 2012), the experts reconvened and reviewed all available data on diesel exhaust and cancer. They concluded that there was sufficient evidence that diesel engine exhaust can cause lung cancer. Their review also showed that there was limited evidence showing a link between diesel exhausts and bladder cancers. The experts retained gasoline exhaust in the 'possibly carcinogenic to humans' category which has remained unchanged from the previous evaluation. With the ubiquitous presence of diesel fuel exhaust in the environment contributed by vehicles and power generators and other occupational exposure, the implications of the findings is colossal. The reclassification puts diesel exhausts in the same category as asbestos and tobacco smoke well known lung carcinogens (cancer causing agents). Lung cancer is the most common cancer in the world and the most common cause of death from cancer, with 1.38 million deaths, with the majority of the cases now occuring in the developing countries (55%) which, apart from tobacco consumption, could be attributed to rapid industrialisation and low regulatory standards for vehicular emissions.

 

In the press release Dr Christopher Portier, Chairman of the IARC working group, said “The scientific evidence was compelling and the Working Group’s conclusion was unanimous: diesel engine exhaust causes lung cancer in humans. Given the additional health impacts from diesel particulates, exposure to this mixture of chemicals should be reduced worldwide.”

One question that emerges is why did it take so long for such a reclassification?  But more importantly, what are we going to do about it now?

Photos: Ruth Stephen 

References:

Silverman DT, Samanic CM, Lubin JH, Blair AE, Stewart PA, Vermeulen R, Coble JB, Rothman N, Schleiff PL, Travis WD, Ziegler RG, Wacholder S, & Attfield MD (2012). The diesel exhaust in miners study: a nested case-control study of lung cancer and diesel exhaust. Journal of the National Cancer Institute, 104 (11), 855-68 PMID: 22393209

Attfield MD, Schleiff PL, Lubin JH, Blair A, Stewart PA, Vermeulen R, Coble JB, & Silverman DT (2012). The diesel exhaust in miners study: a cohort mortality study with emphasis on lung cancer. Journal of the National Cancer Institute, 104 (11), 869-83 PMID: 22393207

Exposure of mothers to pesticides could lead to obesity in children

Environmental agents be it dietary factors, chemicals- drugs, pesticides etc. affect the genetic make-up of individuals. Conversely, changes in the genetic make-up influence variation in individual response to similar environmental agent exposure making some individuals at increased risk for developing certain diseases. Interactions between genes and environmental agents are responsible for most diseases (http://www.niehs.nih.gov/health/topics/science/gene-env/index.cfm). It is also known that exposure of expectant mothers to environmental factors affects the development of diseases in the children. A previous post explored this aspect. http://ecoratorio.blogspot.co.uk/2010/04/paper-of-week-effects-of-prenatal.html

A recent paper (Andersen et al , 2012)  ties all these facts and shows that prenatal exposure to pesticides could affect risk of cardiovascular disease development later in life. Results from a Danish study, which is a part of an on-going prospective study of the effects of pesticide exposure in early pregnancy on the growth and development in the children, offers important insight. From 1996 to 2000 pregnant women working in greenhouses, were recruited consecutively in this study and were categorized as high, medium, or not exposed to pesticides. The children underwent a physical examination at age 6 to11 years that measured blood pressure, body weight, BMI etc. The presence of a gene PON1 and the different types of this gene in the children was also studied.This gene codes for the enzyme HDL-associated  paraoxonase 1 (PON1) has anti-oxidative functions that may protect against atherosclerosis. Additionally it hydrolyses many substrates including organophosphate pesticides. Changes in PON1 ( a common polymorphism- PON1 Q192R) affects both properties. Children with PON1 192R-allele of women exposed to pesticides had higher body fat content, BMI-scores, blood pressure and increased abdominal girth than unexposed children. For children with the PON1 192QQ genotype, exposure of pesticide exposure prenatally had no effect.

This study highlights the complications in gene-environment interactions and  how maternal pesticide exposure can put children with a certain genetic make up  at risk for developing cardiovascular diseases.

Image: Timothy Whallett 

References: Andersen HR, Wohlfahrt-Veje C, Dalgård C, Christiansen L, Main KM, Nellemann C, Murata K, Jensen TK, Skakkebæk NE, & Grandjean P (2012). Paraoxonase 1 polymorphism and prenatal pesticide exposure associated with adverse cardiovascular risk profiles at school age. PloS one, 7 (5) PMID: 22615820

Little monkeys need lots of space

This charming little creature is a White headed marmoset or "Sagui" (Callithrix geoffroyi). Tolerant of humans, they are often seen by tourists and will readily take pieces of fruit in their little hands. Classified as Least Concern (LC) on the IUCN Red List and in appendix II of CITES, surely conservation is no problem? Well, more or less.

Historically many were taken from the wild as pets, their very tolerance of man acting against them. This is tightly controlled these days, but their numbers are still decreasing. In the 21st century loss of habitat is the major problem, or more specifically, fragmentation of habitat. You might think that 20 forests of 1 km sq.would hold the same number of monkeys as 1 of 20 km sq. Indeed, given that predators tend to require much larger ranges and so are less likely to occur in small pockets, you might assume there would be more monkeys. You would be wrong (Chiarello & de Melo, 2001). There are various reasons.

a) Long term of course, small populations lack enough genetic diversity to stay healthy, but there are more immediate reasons.

b) Small forest fragments tend to favour trees and shrubs which are forest edge species, with proportionally less canopy or forest interior species (Cardoso da Silva and Tabarelli, 2000). Unfortunately, these are the very ones that produce the most fruit. Thus small monkeys, which tend to need a lot of fruit, suffer accordingly. In the same way, large fruit eating birds like macaws and toucans tend to be absent from isolated forests less than 250 hectares (Willis 1979).

Our little saguis are quite adaptable, and eat a lot of tree gum and insects (and anything really), so suffer less than fruit eating specialists, but it still cuts down their options. And they have another problem.

c). Small fragments may have fewer large fragments, but they still have plenty of cats, either native or feral from surrounding farm and residential land. Saguis and other small monkeys are especially susceptible to cats. They do their best, mobbing them and screeching, but that's not always enough. As an aside, it has been shown that being part of a "mob" actually reduces rather than increases monkey stress - it is tempting to extrapolate that to humans!

Driving through a landscape of fields and copses may appear more "natural" than a prairie of wheat or sugar cane, and it is, but maybe not that much more.

References
Cardoso da Silva JM, & Tabarelli M (2000). Tree species impoverishment and the future flora of the Atlantic forest of northeast Brazil. Nature, 404 (6773), 72-4 PMID: 10716443
Chiarello, A.G., de Melo, F.R. (2001). Primate population densities and sizes in Atlantic forest remnants of northern Espirito Santo, Brazil. International Journal of Primatology, 22, 379-396.

Willis, E.O. (1979). The composition of avian communities in remanescent woodlots in southern Brazil. Papéis Avulsos de Zoologia, São Paulo, 33, 1-25.